AIM: To investigate the effect of gastrodin on the expression of brain-derived neurotrophic factor (BDNF) and interleukin-6 (IL-6) in the striatum of cerebral ischemia rats, and to explore the potential mechanism of gastrodin in treating cerebral ischemia. METHODS: The rats were randomly divided into four groups: normal, sham, model, and gastrodin groups, each consisting of 10 rats. After successful modeling using middle cerebral artery occlusion (MCAO), the gastrodin group received intraperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days. Pathological changes in striatal neurons were observed using Nissl staining. Immunohistochemistry was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum. Additionally, immunoblot analysis was performed to determine the expression levels of BDNF and IL-6 proteins in the striatum. RESULTS: Nissl staining revealed clear and intact structures of striatal neurons in the normal and sham groups, with tightly arranged cells. In the model group, the number of cells was significantly reduced compared to the sham group (P<0.01), and there was a noticeable cytosolic atrophy and loose cell arrangement. The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group (P<0.01), and there was also a significant improvement in cell morphology. The results of immunohistochemistry and immunoblot were consistent, and there was no statistically significant difference in BDNF and IL-6 protein expression between the normal group and the sham group (P>0.05). Compared to the sham group, the model group showed a decrease in the protein expression level of BDNF in the striatum on the ischemic side (P<0.01) and an increase in the protein expression level of IL-6 (P<0.05, P<0.01). In contrast, the gastrodin group showed an increase in the protein expression level of BDNF in the striatum on the ischemic side (P<0.05, P<0.01) and a decrease in the protein expression level of IL-6 (P< 0.05, P<0.01) compared to the model group. CONCLUSION: Gastrodin has a significant protective effect on striatal injury caused by cerebral ischemia, and its mechanism may be related to the up-regulation of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

Endometriosis is a common chronic gynecological disease with endometrial cell implantation outside the uterus.Angiogenesis is a major pathophysiology in endometriosis.Our previous studies have demon-strated that the prodrug of epigallocatechin gallate(ProEGCG)exhibits superior anti-endometriotic and anti-angiogenic effects compared to epigallocatechin gallate(EGCG).However,their direct binding targets and underlying mechanisms for the differential effects remain unknown.In this study,we demonstrated that oral ProEGCG can be effective in preventing and treating endometriosis.Additionally,1D and 2D Proteome Integral Solubility Alteration assay-based chemical proteomics identified metadherin(MTDH)and PX domain containing serine/threonine kinase-like(PXK)as novel binding targets of EGCG and ProEGCG,respectively.Computational simulation and BioLayer interferometry were used to confirm their binding affinity.Our results showed that MTDH-EGCG inhibited protein kinase B(Akt)-mediated angiogenesis,while PXK-ProEGCG inhibited epidermal growth factor(EGF)-mediated angiogenesis via the EGF/hypoxia-inducible factor(HIF-1a)/vascular endothelial growth factor(VEGF)pathway.In vitro and in vivo knockdown assays and microvascular network imaging further confirmed the involvement of these signaling pathways.Moreover,our study demonstrated that ProEGCG has superior therapeutic effects than EGCG by targeting distinct signal transduction pathways and may act as a novel anti-angiogenic therapy for endometriosis.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.